Elsner, Leslie

[["cris.virtual.author-orcid","0000-0002-1651-1214"],["cris.virtual.author-orcid","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtual.author-orcid","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtual.author-orcid","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtual.author-orcid","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtual.department","Universitätsmedizin Göttingen"],["cris.virtual.department","Universitätsmedizin Göttingen"],["cris.virtual.department","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtual.department","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtual.department","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtualsource.author-orcid","b8e6502e-ec7d-43b8-89c1-27118d7c9bb2"],["cris.virtualsource.author-orcid","11b2f35d-3b48-45e1-b088-02271c68aaa1"],["cris.virtualsource.author-orcid","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtualsource.author-orcid","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtualsource.author-orcid","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtualsource.department","b8e6502e-ec7d-43b8-89c1-27118d7c9bb2"],["cris.virtualsource.department","11b2f35d-3b48-45e1-b088-02271c68aaa1"],["cris.virtualsource.department","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtualsource.department","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtualsource.department","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["dc.bibliographiccitation.firstpage","1005"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","The Journal of Immunology"],["dc.bibliographiccitation.lastpage","1014"],["dc.bibliographiccitation.volume","185"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Novota, Peter"],["dc.contributor.author","Kanwar, Namita"],["dc.contributor.author","von Mollard, Gabriele Fischer"],["dc.date.accessioned","2018-11-07T08:41:22Z"],["dc.date.available","2018-11-07T08:41:22Z"],["dc.date.issued","2010"],["dc.description.abstract","The exocytosis of cytotoxic proteins stored in lytic granules of activated CTL is a key event during killing of target cells. Membrane fusion events that are mediated by soluble N-ethylmaleimide-sensitive-factor attachment protein receptor (SNARE) proteins are crucial, as demonstrated by patients with familial hemophagocytic lymphohistocytosis type 4 who have mutations in the SNARE protein syntaxin-11 that result in an impaired degranulation of cytotoxic cells. We found an increased mRNA expression of the SNARE protein genes Vti1b and Vamp8 during Ag-specific activation of CTL from TCR-transgenic OT-I mice. Therefore, we investigated the cytolytic activity of CTL from TCR-transgenic Vti1b and Vamp8 knockout mice. At 3 d as well as at 4 d of Ag-specific stimulation, the degranulation of CTL was significantly reduced in Vti1b and Vamp8 knockout mice, as determined by cell surface expression of the degranulation marker CD107a. After 3 d of Ag-specific stimulation, the cytolytic activity of Vti1b- and Vamp8-deficient CTL was reduced to approximate to 50% compared with heterozygous controls. However, 4 d after stimulation, the cytotoxic activity of Vti1b- as well as Vamp8-deficient CTL was not impaired anymore. The capacity of Vti1b- and Vamp8-deficient dendritic cells to process Ags and to stimulate the proliferation of CTL was not reduced, arguing against an indirect effect on the activation of CTL. These findings suggest a role of the SNARE proteins vti1b and vesicle-associated membrane protein 8 in the degranulation of CTL. However, a deficiency can apparently be compensated and affects only transiently the cytotoxic activity of CTL during their development to armed effector cells. The Journal of Immunology, 2010, 185: 1005-1014."],["dc.identifier.doi","10.4049/jimmunol.1000770"],["dc.identifier.isi","000279675200028"],["dc.identifier.pmid","20543108"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19451"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Immunologists"],["dc.relation.issn","0022-1767"],["dc.title","The Exocytosis of Lytic Granules Is Impaired in Vti1b- or Vamp8-Deficient CTL Leading to a Reduced Cytotoxic Activity following Antigen-Specific Activation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["cris.virtual.author-orcid","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtual.author-orcid","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtual.author-orcid","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtual.author-orcid","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtual.author-orcid","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtual.author-orcid","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtual.author-orcid","0000-0003-1190-4040"],["cris.virtual.author-orcid","0000-0002-1651-1214"],["cris.virtual.department","Universitätsmedizin Göttingen"],["cris.virtual.department","Universitätsmedizin Göttingen"],["cris.virtual.department","Universitätsmedizin Göttingen"],["cris.virtual.department","Universitätsmedizin Göttingen"],["cris.virtual.department","Universitätsmedizin Göttingen"],["cris.virtual.department","#PLACEHOLDER_PARENT_METADATA_VALUE#"],["cris.virtual.department","Institut für Pharmakologie und Toxikologie"],["cris.virtual.department","Universitätsmedizin Göttingen"],["cris.virtualsource.author-orcid","bfb9620f-7265-426d-ad01-b0b69d13e6e5"],["cris.virtualsource.author-orcid","31870ba4-f58d-4096-b2fa-f1cead8d77c9"],["cris.virtualsource.author-orcid","d7d98060-8082-46e8-972f-2dfab1b501cc"],["cris.virtualsource.author-orcid","bf6f60ce-9405-4ab7-86c0-3ed9f441d244"],["cris.virtualsource.author-orcid","11b2f35d-3b48-45e1-b088-02271c68aaa1"],["cris.virtualsource.author-orcid","b88f3c2c-2563-4a4a-843e-a926abfe7876"],["cris.virtualsource.author-orcid","bb4ea395-7131-470f-8440-c9ba13eb663e"],["cris.virtualsource.author-orcid","b8e6502e-ec7d-43b8-89c1-27118d7c9bb2"],["cris.virtualsource.department","bfb9620f-7265-426d-ad01-b0b69d13e6e5"],["cris.virtualsource.department","31870ba4-f58d-4096-b2fa-f1cead8d77c9"],["cris.virtualsource.department","d7d98060-8082-46e8-972f-2dfab1b501cc"],["cris.virtualsource.department","bf6f60ce-9405-4ab7-86c0-3ed9f441d244"],["cris.virtualsource.department","11b2f35d-3b48-45e1-b088-02271c68aaa1"],["cris.virtualsource.department","b88f3c2c-2563-4a4a-843e-a926abfe7876"],["cris.virtualsource.department","bb4ea395-7131-470f-8440-c9ba13eb663e"],["cris.virtualsource.department","b8e6502e-ec7d-43b8-89c1-27118d7c9bb2"],["dc.bibliographiccitation.artnumber","924"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Johannsen, Hannah"],["dc.contributor.author","Muppala, Vijayakumar"],["dc.contributor.author","Gröschel, Carina"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Didié, Michael"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2018-04-23T11:49:21Z"],["dc.date.available","2018-04-23T11:49:21Z"],["dc.date.issued","2017"],["dc.description.abstract","The perspective to transplant grafts derived from pluripotent stem cells has gained much attention in recent years. Parthenogenetic stem cells (PSCs) are an alternative pluripotent stem cell type that is attractive as source of grafts for allogeneic transplantations because most PSCs are haploidentical for the major histocompatibility complex (MHC). This reduced immunogenetic complexity of PSCs could tremendously simplify the search for MHC-matched allogeneic stem cells. In this study, we have characterized immunological properties of the MHC haploidentical PSC line A3 (H2d/d) and the heterologous PSC line A6 (H2b/d). Both PSC lines largely lack MHC class I molecules, which present peptides to cytotoxic T lymphocytes (CTLs) and serve as ligands for inhibitory natural killer (NK) receptors. They express ligands for activating NK receptors, including the NKG2D ligand RAE-1, and the DNAM-1 ligands CD112 and CD155. Consequently, both PSC lines are highly susceptible to killing by IL-2-activated NK cells. In vitro-differentiated cells acquire resistance and downregulate ligands for activating NK receptors but fail to upregulate MHC class I molecules. The PSC line A6 and differentiated A6 cells are largely resistant to CTLs derived from T cell receptor transgenic OT-I mice after pulsing of the targets with the appropriate peptide. The high susceptibility to killing by activated NK cells may constitute a general feature of pluripotent stem cells as it has been also found with other pluripotent stem cell types. This activity potentially increases the safety of transplantations, if grafts contain traces of undifferentiated cells that could be tumorigenic in the recipient."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.3389/fimmu.2017.00924"],["dc.identifier.gro","3142522"],["dc.identifier.pmid","28824647"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14593"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13678"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/213"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | C05: Bedeutung von zellulären Immunreaktionen für das kardiale Remodeling und die Therapie der Herzinsuffizienz durch Stammzelltransplantation"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.issn","1664-3224"],["dc.relation.workinggroup","RG Dressel"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Immunological Properties of Murine Parthenogenetic Stem Cells and Their Differentiation Products"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Tissue Antigens"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Hamann, Carina"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Nolte, Jessica"],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2018-11-07T09:38:32Z"],["dc.date.available","2018-11-07T09:38:32Z"],["dc.date.issued","2014"],["dc.format.extent","5"],["dc.identifier.isi","000337546000002"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33083"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.eventlocation","Stockholm, SWEDEN"],["dc.relation.issn","1399-0039"],["dc.relation.issn","0001-2815"],["dc.title","PLURIPOTENT STEM CELLS VARYING IN A SINGLE MINOR HISTOCOMPATIBILITY ANTIGEN ELICIT CELLULAR AND HUMORAL IMMUNE RESPONSES THAT CAN MEDIATE GRAFT REJECTION"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5523"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","The Journal of Immunology"],["dc.bibliographiccitation.lastpage","5533"],["dc.bibliographiccitation.volume","179"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Muppala, Vijayakumar"],["dc.contributor.author","Gehrmann, Mathias"],["dc.contributor.author","Lozano, Jingky"],["dc.contributor.author","Malzahn, Dörthe"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Brunner, Edgar"],["dc.contributor.author","Zientkowska, Marta"],["dc.contributor.author","Herrmann, Thomas"],["dc.contributor.author","Walter, Lutz"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2022-06-08T07:57:36Z"],["dc.date.available","2022-06-08T07:57:36Z"],["dc.date.issued","2007"],["dc.description.abstract","The stress-inducible heat shock protein (HSP) 70 is known to function as an endogenous danger signal that can increase the immunogenicity of tumors and induce CTL responses. We show in this study that HSP70 also activates mouse NK cells that recognize stress-inducible NKG2D ligands on tumor cells. Tumor size and the rate of metastases derived from HSP70-overexpressing human melanoma cells were found to be reduced in T and B cell-deficient SCID mice, but not in SCID/beige mice that lack additionally functional NK cells. In the SCID mice with HSP70-overexpressing tumors, NK cells were activated so that they killed ex vivo tumor cells that expressed NKG2D ligands. In the tumors, the MHC class I chain-related (MIC) A and B molecules were found to be expressed. Interestingly, a counter selection was observed against the expression of MICA/B in HSP70-overexpressing tumors compared with control tumors in SCID, but not in SCID/beige mice, suggesting a functional relevance of MICA/B expression. The melanoma cells were found to release exosomes. HSP70-positive exosomes from the HSP70-overexpressing cells, in contrast to HSP70-negative exosomes from the control cells, were able to activate mouse NK cells in vitro to kill YAC-1 cells, which express NKG2D ligands constitutively, or the human melanoma cells, in which MICA/B expression was induced. Thus, HSP70 and inducible NKG2D ligands synergistically promote the activation of mouse NK cells resulting in a reduced tumor growth and suppression of metastatic disease."],["dc.identifier.doi","10.4049/jimmunol.179.8.5523"],["dc.identifier.isi","000250099400061"],["dc.identifier.pmid","17911639"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/110150"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-575"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation.eissn","1550-6606"],["dc.relation.issn","0022-1767"],["dc.title","The Heat Shock Protein HSP70 Promotes Mouse NK Cell Activity against Tumors That Express Inducible NKG2D Ligands"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","497"],["dc.bibliographiccitation.lastpage","512"],["dc.bibliographiccitation.seriesnr","631"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2021-04-21T11:15:34Z"],["dc.date.available","2021-04-21T11:15:34Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/bs.mie.2019.05.037"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84259"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/335"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C05: Bedeutung von zellulären Immunreaktionen für das kardiale Remodeling und die Therapie der Herzinsuffizienz durch Stammzelltransplantation"],["dc.relation.crisseries","Methods in Enzymology"],["dc.relation.isbn","9780128186732"],["dc.relation.ispartof","Tumor Immunology and Immunotherapy – Cellular Methods Part A"],["dc.relation.ispartofseries","Methods in Enzymology; 631"],["dc.relation.workinggroup","RG Dressel"],["dc.title","51Cr-release to monitor NK cell cytotoxicity"],["dc.type","book_chapter"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","109"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Immunogenetics"],["dc.bibliographiccitation.lastpage","123"],["dc.bibliographiccitation.volume","68"],["dc.contributor.author","Isernhagen, Antje"],["dc.contributor.author","Schilling, Daniela"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Shah, Pranali"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Walter, Lutz"],["dc.contributor.author","Multhoff, Gabriele"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2018-11-07T10:18:55Z"],["dc.date.available","2018-11-07T10:18:55Z"],["dc.date.issued","2016"],["dc.description.abstract","The MHC class I chain-related molecule A (MICA) is a ligand for the activating natural killer (NK) cell receptor NKG2D. A polymorphism causing a valine to methionine exchange at position 129 affects binding to NKG2D, cytotoxicity, interferon-gamma release by NK cells and activation of CD8(+) T cells. It is known that tumors can escape NKG2D-mediated immune surveillance by proteolytic shedding of MICA. Therefore, we investigated whether this polymorphism affects plasma membrane expression (pmMICA) and shedding of MICA. Expression of pmMICA was higher in a panel of tumor (n = 16, P = 0.0699) and melanoma cell lines (n = 13, P = 0.0429) carrying the MICA-129Val/Val genotype. MICA-129Val homozygous melanoma cell lines released more soluble MICA (sMICA) by shedding (P = 0.0015). MICA-129Met or MICA-129Val isoforms differing only in this amino acid were expressed in the MICA-negative melanoma cell line Malme, and clones with similar pmMICA expression intensity were selected. The MICA-129Met clones released more sMICA (P = 0.0006), and a higher proportion of the MICA-129Met than the MICA-129Val variant was retained in intracellular compartments (P = 0.0199). The MICA-129Met clones also expressed more MICA messenger RNA (P = 0.0047). The latter phenotype was also observed in mouse L cells transfected with the MICA expression constructs (P = 0.0212). In conclusion, the MICA-129Met/Val dimorphism affects the expression density of MICA on the plasma membrane. More of the MICA-129Met variants were retained intracellularly. If expressed at the cell surface, the MICA-129Met isoform was more susceptible to shedding. Both processes appear to limit the cell surface expression of MICA-129Met variants that have a high binding avidity to NKG2D."],["dc.identifier.doi","10.1007/s00251-015-0884-8"],["dc.identifier.isi","000369012800002"],["dc.identifier.pmid","26585323"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12585"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41550"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/128"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C05: Bedeutung von zellulären Immunreaktionen für das kardiale Remodeling und die Therapie der Herzinsuffizienz durch Stammzelltransplantation"],["dc.relation.issn","1432-1211"],["dc.relation.issn","0093-7711"],["dc.relation.workinggroup","RG Dressel"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The MICA-129Met/Val dimorphism affects plasma membrane expression and shedding of the NKG2D ligand MICA"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1480"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.lastpage","1502"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Isernhagen, Antje"],["dc.contributor.author","Malzahn, Doerthe"],["dc.contributor.author","Viktorova, Elena"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","von Bonin, Frederike"],["dc.contributor.author","Kilisch, Markus"],["dc.contributor.author","Wermuth, Janne Marieke"],["dc.contributor.author","Walther, Neele"],["dc.contributor.author","Balavarca, Yesilda"],["dc.contributor.author","Stahl-Hennig, Christiane"],["dc.contributor.author","Engelke, Michael"],["dc.contributor.author","Walter, Lutz"],["dc.contributor.author","Bickeboeller, Heike"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2018-11-07T09:49:36Z"],["dc.date.available","2018-11-07T09:49:36Z"],["dc.date.issued","2015"],["dc.description.abstract","The MHC class I chain-related molecule A (MICA) is a highly polymorphic ligand for the activating natural killer (NK)-cell receptor NKG2D. A single nucleotide polymorphism causes a valine to methionine exchange at position 129. Presence of a MICA-129Met allele in patients (n=452) undergoing hematopoietic stem cell transplantation (HSCT) increased the chance of overall survival (hazard ratio [HR]=0.77, P=0.0445) and reduced the risk to die due to acute graft-versus-host disease (aGVHD) (odds ratio [OR]=0.57, P=0.0400) although homozygous carriers had an increased risk to experience this complication (OR=1.92, P=0.0371). Overall survival of MICA-129Val/Val genotype carriers was improved when treated with anti-thymocyte globulin (HR=0.54, P=0.0166). Functionally, the MICA-129Met isoform was characterized by stronger NKG2D signaling, triggering more NK-cell cytotoxicity and interferon- release, and faster co-stimulation of CD8(+) T cells. The MICA-129Met variant also induced a faster and stronger down-regulation of NKG2D on NK and CD8(+) T cells than the MICA-129Val isoform. The reduced cell surface expression of NKG2D in response to engagement by MICA-129Met variants appeared to reduce the severity of aGVHD."],["dc.description.sponsorship","Open-Access Publikationsfonds 2015"],["dc.identifier.doi","10.15252/emmm.201505246"],["dc.identifier.isi","000364320100008"],["dc.identifier.pmid","26483398"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12462"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35542"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/127"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C05: Bedeutung von zellulären Immunreaktionen für das kardiale Remodeling und die Therapie der Herzinsuffizienz durch Stammzelltransplantation"],["dc.relation.issn","1757-4684"],["dc.relation.issn","1757-4676"],["dc.relation.workinggroup","RG Dressel"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The MICA-129 dimorphism affects NKG2D signaling and outcome of hematopoietic stem cell transplantation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e2622"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Schindehuette, Jan"],["dc.contributor.author","Kuhlmann, Tanja"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Novota, Peter"],["dc.contributor.author","Baier, Paul Christian"],["dc.contributor.author","Schillert, Arne"],["dc.contributor.author","Bickeboeller, Heike"],["dc.contributor.author","Herrmann, Thomas R."],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Mansouri, Ahmed"],["dc.date.accessioned","2018-11-07T11:13:02Z"],["dc.date.available","2018-11-07T11:13:02Z"],["dc.date.issued","2008"],["dc.description.abstract","Embryonic stem (ES) cells have the potential to differentiate into all cell types and are considered as a valuable source of cells for transplantation therapies. A critical issue, however, is the risk of teratoma formation after transplantation. The effect of the immune response on the tumorigenicity of transplanted cells is poorly understood. We have systematically compared the tumorigenicity of mouse ES cells and in vitro differentiated neuronal cells in various recipients. Subcutaneous injection of 1 x 10(6) ES or differentiated cells into syngeneic or allogeneic immunodeficient mice resulted in teratomas in about 95% of the recipients. Both cell types did not give rise to tumors in immunocompetent allogeneic mice or xenogeneic rats. However, in 61% of cyclosporine A-treated rats teratomas developed after injection of differentiated cells. Undifferentiated ES cells did not give rise to tumors in these rats. ES cells turned out to be highly susceptible to killing by rat natural killer (NK) cells due to the expression of ligands of the activating NK receptor NKG2D on ES cells. These ligands were downregulated on differentiated cells. The activity of NK cells which is not suppressed by cyclosporine A might contribute to the prevention of teratomas after injection of ES cells but not after inoculation of differentiated cells. These findings clearly point to the importance of the immune response in this process. Interestingly, the differentiated cells must contain a tumorigenic cell population that is not present among ES cells and which might be resistant to NK cell-mediated killing."],["dc.identifier.doi","10.1371/journal.pone.0002622"],["dc.identifier.isi","000264065800024"],["dc.identifier.pmid","18612432"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8264"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53801"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","The Tumorigenicity of Mouse Embryonic Stem Cells and In Vitro Differentiated Neuronal Cells Is Controlled by the Recipients' Immune Response"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2164"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","The FASEB journal"],["dc.bibliographiccitation.lastpage","2177"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Nolte, Jessica"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Novota, Peter"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Streckfuss-Boemeke, Katrin"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Jaenisch, Rudolf"],["dc.contributor.author","Engel, Wolfgang"],["dc.date.accessioned","2017-09-07T11:45:57Z"],["dc.date.available","2017-09-07T11:45:57Z"],["dc.date.issued","2010"],["dc.description.abstract","Multipotent adult germ-line stem cells (maGSCs) and induced pluripotent stem cells (iPSCs) could be used to generate autologous cells for therapeutic purposes, which are expected to be tolerated by the recipient. However, effects of the immune system on these cells have not been investigated. We have compared the susceptibility of maGSC lines to IL-2-activated natural killer (NK) cells with embryonic stem cell (ESC) lines, iPSCs, and F9 teratocarcinoma cells. The killing of pluripotent cell lines by syngeneic, allogeneic, and xenogeneic killer cells ranged between 48 and 265% in chromium release assays when compared to YAC-1 cells, which served as highly susceptible reference cells. With the exception of 2 maGSC lines, they expressed ligands for the activating NK receptor NKG2D that belong to the RAE-1 family, and killing could be inhibited by soluble NKG2D, demonstrating a functional role of these molecules. Furthermore, ligands of the activating receptor DNAM-1 were frequently expressed. The susceptibility to NK cells might constitute a common feature of pluripotent cells. It could result in rejection after transplantation, as suggested by a reduced teratoma growth after NK cell activation in vivo, but it might also offer a strategy to deplete contaminating pluripotent cells before grafting of differentiated cells.-Dressel, R., Nolte, J., Elsner, L., Novota, P., Guan, K., Streckfuss-Bomeke, K., Hasenfuss, G., Jaenisch, R., Engel, W. Pluripotent stem cells are highly susceptible targets for syngeneic, allogeneic, and xenogeneic natural killer cells. FASEB J. 24, 2164-2177 (2010). www.fasebj.org"],["dc.identifier.doi","10.1096/fj.09-134957"],["dc.identifier.gro","3142896"],["dc.identifier.isi","000279343600004"],["dc.identifier.pmid","20145206"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6231"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/351"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Federation Amer Soc Exp Biol"],["dc.relation.issn","0892-6638"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Pluripotent stem cells are highly susceptible targets for syngeneic, allogeneic, and xenogeneic natural killer cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","2665"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Gröschel, Carina"],["dc.contributor.author","Sasse, André"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Röhrborn, Charlotte"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Didié, Michael"],["dc.contributor.author","Reupke, Verena"],["dc.contributor.author","Bunt, Gertrude"],["dc.contributor.author","Lichtman, Andrew H."],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2019-07-09T11:49:35Z"],["dc.date.available","2019-07-09T11:49:35Z"],["dc.date.issued","2018"],["dc.description.abstract","Heart failure due to pressure overload is frequently associated with inflammation. In addition to inflammatory responses of the innate immune system, autoimmune reactions of the adaptive immune system appear to be triggered in subgroups of patients with heart failure as demonstrated by the presence of autoantibodies against myocardial antigens. Moreover, T cell-deficient and T cell-depleted mice have been reported to be protected from heart failure induced by transverse aortic constriction (TAC) and we have shown recently that CD4+-helper T cells with specificity for an antigen in cardiomyocytes accelerate TAC-induced heart failure. In this study, we set out to investigate the potential contribution of CD8+-cytotoxic T cells with specificity to a model antigen (ovalbumin, OVA) in cardiomyocytes to pressure overload-induced heart failure. In 78% of cMy-mOVA mice with cardiomyocyte-specific OVA expression, a low-grade OVA-specific cellular cytotoxicity was detected after TAC. Adoptive transfer of OVA-specific CD8+-T cells from T cell receptor transgenic OT-I mice before TAC did not increase the risk of OVA-specific autoimmunity in cMy-mOVA mice. After TAC, again 78% of the mice displayed an OVA-specific cytotoxicity with on average only a three-fold higher killing of OVA-expressing target cells. More CD8+ cells were present after TAC in the myocardium of cMy-mOVA mice with OT-I T cells (on average 17.5/mm2) than in mice that did not receive OVA-specific CD8+-T cells (3.6/mm2). However, the extent of fibrosis was similar in both groups. Functionally, as determined by echocardiography, the adoptive transfer of OVA-specific CD8+-T cells did not significantly accelerate the progression from hypertrophy to heart failure in cMy-mOVA mice. These findings argue therefore against a major impact of cytotoxic T cells with specificity for autoantigens of cardiomyocytes in pressure overload-induced heart failure."],["dc.identifier.doi","10.3389/fimmu.2018.02665"],["dc.identifier.pmid","30498501"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15720"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59587"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/298"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | C05: Bedeutung von zellulären Immunreaktionen für das kardiale Remodeling und die Therapie der Herzinsuffizienz durch Stammzelltransplantation"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.workinggroup","RG Dressel"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","CD8+-T Cells With Specificity for a Model Antigen in Cardiomyocytes Can Become Activated After Transverse Aortic Constriction but Do Not Accelerate Progression to Heart Failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]